The following proposal will extend our understanding of interactions between cardiovascular and somatosensory regulatory systems by determine whether acute or chronic changes in blood pressure alter reactivity to nonaversive, tactile stimulation as measured by the startle response to airpuff stimuli. Data linking cardiovascular with pain-inhibitory systems suggest that regulation off blood pressure acts to modify pain sensitivity. Work in our laboratory suggests that reactivity in other somatosensory modalities may also be determined by mechanisms that participate in the homeostatic control of blood pressure. We recently found that normotensive rats with higher blood pressure have higher Thresholds for tactile stimulation than rats with lower pressure, and that tactile reactivity is attenuated in experimental hypertension. The possibility that cardiovascular regulatory systems modulate sensitivity across somatosensory modalities leads to the hypothesis that reactivity to nonaversive. tactile stimuli will be attenuated tactile reactivity to nonaversive,, tactile stimuli will be attenuated by acute or chronic increases in blood pressure. ?he current proposal will examine tactile reactivity following acute and chronic manipulations of blood pressure in Dahl salt-sensitive (S) rats, which remain normotensive when maintained on low dietary salt (0.3% NaC1) but develop hypertension when exposed to high salt (8% NaC1), and in Dahl salt-resistant (R) rats, which remain normotensive regardless of hypertension to determine (1) whether there is a genetic component to tactile startle reactivity and (2) whether tactile startle is attenuated when blood pressure is elevated acutely by infusion of the pressor agent phenylephrine hydrochloride, an alpha-adrenergic receptor agonist. In additional experiments, 33 days to ascertain (3) whether either high blood pressure or intake of excess sodium chloride affects reactivity and (4) whether decreased reactivity will be produced by acutely reducing blood pressure with the depressor agent sodium nitroprusside, a direct-acting vasodilator. These studies will delineate the impact of blood pressure on somatosensory reactivity to nonaversive stimuli, thus addressing the possibility that hypertension may cause widespread sensory deficits.